LncRNA MT1DP Aggravates Cadmium-Induced Oxidative Stress by Repressing the Function of Nrf2 and is Dependent on Interaction with miR-365

doi:10.1002/advs.201800087

	LncRNA MT1DP Aggravates Cadmium-Induced Oxidative Stress by Repressing the Function of Nrf2 and is Dependent on Interaction with miR-365
	Gao, Ming 1,2; Li, Changying 3; Xu, Ming1,2 ; Liu, Yun1,4 ; Cong, Min 3; Liu, Sijin 1,2
	2018-07-01
发表期刊	ADVANCED SCIENCE
ISSN	2198-3844
通讯作者	Liu, Sijin(sjliu@rcees.ac.cn)
摘要	Although cadmium (Cd)-induced hepatoxicity is well established, pronounced knowledge gaps remain existed regarding the inherent cellular signaling that dictates Cd toxicity. Specifically, the molecular basis for determining the equilibrium between prosurvival and proapoptotic signaling remains poorly understood. Thus, it is recently revealed that long non-coding RNA (lncRNA) MT1DP, a pseudogene in the metallothionein (MT) family, promoted Cd-induced cell death through activating the RhoC-CCN1/2-AKT pathway and modulating MT1H induction. Here, first the dependency of MT1DP induction on MTF1, an important transcriptional factor in driving the mRNA expression of MT1 members is defined. Additionally, a bridge molecule between MT1DP and nuclear factor erythroid 2-related factor 2 (Nrf2) is established: miR-365. Mechanistically, MT1DP induction under Cd stress decreases the nuclear factor erythroid 2-related factor 2 (Nrf2) level to evoke oxidative stress through the elevation of miR-365, which acted to repress the Nrf2 level via direct binding to its 3'UTR. In contrast to the competing endogenous RNA (ceRNA) mechanism, a new mechanism is proposed: MT1DP elevated the miR-365 level though stabilizing its RNA via direct binding. Collectively, the combined data demonstrate a crucial role of MT1DP in reducing the Nrf2-mediated protection of cells, and this is dependent on the interplay with miR-365. Hence, the study further expands the knowledge of inducible endogenous lncRNA in modulating oxidative stress.
关键词	cadmium long non-coding RNA (lncRNA) miR-365 MT1DP Nrf2 oxidative stress
DOI	10.1002/advs.201800087
关键词[WOS]	LONG NONCODING RNA ; ERYTHROID-CELLS ; FACTOR-I ; TOXICITY ; LIVER ; GENE ; MECHANISMS ; EXPRESSION ; PATHWAYS ; EXPOSURE
收录类别	SCI
语种	英语
资助项目	Strategic Priority Research Program of the Chinese Academy of Sciences[XDB14000000] ; National Natural Science Foundation of China[21507154] ; National Natural Science Foundation of China[21425731] ; National Natural Science Foundation of China[21637004] ; National Natural Science Foundation of China[81570542] ; national 973 program[2014CB932000] ; Strategic Priority Research Program of the Chinese Academy of Sciences[XDB14000000] ; National Natural Science Foundation of China[21507154] ; National Natural Science Foundation of China[21425731] ; National Natural Science Foundation of China[21637004] ; National Natural Science Foundation of China[81570542] ; national 973 program[2014CB932000]
项目资助者	Strategic Priority Research Program of the Chinese Academy of Sciences ; Strategic Priority Research Program of the Chinese Academy of Sciences ; Strategic Priority Research Program of the Chinese Academy of Sciences ; Strategic Priority Research Program of the Chinese Academy of Sciences ; Strategic Priority Research Program of the Chinese Academy of Sciences ; Strategic Priority Research Program of the Chinese Academy of Sciences ; Strategic Priority Research Program of the Chinese Academy of Sciences ; Strategic Priority Research Program of the Chinese Academy of Sciences ; Strategic Priority Research Program of the Chinese Academy of Sciences ; Strategic Priority Research Program of the Chinese Academy of Sciences ; Strategic Priority Research Program of the Chinese Academy of Sciences ; Strategic Priority Research Program of the Chinese Academy of Sciences ; Strategic Priority Research Program of the Chinese Academy of Sciences ; Strategic Priority Research Program of the Chinese Academy of Sciences ; Strategic Priority Research Program of the Chinese Academy of Sciences ; Strategic Priority Research Program of the Chinese Academy of Sciences ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; national 973 program ; national 973 program ; national 973 program ; national 973 program ; national 973 program ; national 973 program ; national 973 program ; national 973 program ; national 973 program ; national 973 program ; national 973 program ; national 973 program ; national 973 program ; national 973 program ; national 973 program ; national 973 program ; Strategic Priority Research Program of the Chinese Academy of Sciences ; Strategic Priority Research Program of the Chinese Academy of Sciences ; Strategic Priority Research Program of the Chinese Academy of Sciences ; Strategic Priority Research Program of the Chinese Academy of Sciences ; Strategic Priority Research Program of the Chinese Academy of Sciences ; Strategic Priority Research Program of the Chinese Academy of Sciences ; Strategic Priority Research Program of the Chinese Academy of Sciences ; Strategic Priority Research Program of the Chinese Academy of Sciences ; Strategic Priority Research Program of the Chinese Academy of Sciences ; Strategic Priority Research Program of the Chinese Academy of Sciences ; Strategic Priority Research Program of the Chinese Academy of Sciences ; Strategic Priority Research Program of the Chinese Academy of Sciences ; Strategic Priority Research Program of the Chinese Academy of Sciences ; Strategic Priority Research Program of the Chinese Academy of Sciences ; Strategic Priority Research Program of the Chinese Academy of Sciences ; Strategic Priority Research Program of the Chinese Academy of Sciences ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; national 973 program ; national 973 program ; national 973 program ; national 973 program ; national 973 program ; national 973 program ; national 973 program ; national 973 program ; national 973 program ; national 973 program ; national 973 program ; national 973 program ; national 973 program ; national 973 program ; national 973 program ; national 973 program
WOS研究方向	Chemistry ; Science & Technology - Other Topics ; Materials Science
WOS类目	Chemistry, Multidisciplinary ; Nanoscience & Nanotechnology ; Materials Science, Multidisciplinary
WOS记录号	WOS:000439842100017
出版者	WILEY
引用统计	被引频次：61[WOS] [WOS记录] [WOS相关记录]
文献类型	期刊论文
条目标识符	http://ir.hfcas.ac.cn:8080/handle/334002/37691
专题	技术生物与农业工程研究所
通讯作者	Liu, Sijin
作者单位	1.Chinese Acad Sci, Res Ctr Ecoenvironm Sci, State Key Lab Environm Chem & Ecotoxicol, Beijing 100085, Peoples R China 2.Univ Chinese Acad Sci, Coll Resources & Environm, Beijing 100049, Peoples R China 3.Capital Med Univ, Beijing Friendship Hosp, Liver Res Ctr, Beijing 100050, Peoples R China 4.Chinese Acad Sci & Anhui Prov, Hefei Inst Phys Sci, Key Lab Ion Beam Bioengn, Hefei 230031, Anhui, Peoples R China
推荐引用方式 GB/T 7714	Gao, Ming,Li, Changying,Xu, Ming,et al. LncRNA MT1DP Aggravates Cadmium-Induced Oxidative Stress by Repressing the Function of Nrf2 and is Dependent on Interaction with miR-365[J]. ADVANCED SCIENCE,2018,5(7):9.
APA	Gao, Ming,Li, Changying,Xu, Ming,Liu, Yun,Cong, Min,&Liu, Sijin.(2018).LncRNA MT1DP Aggravates Cadmium-Induced Oxidative Stress by Repressing the Function of Nrf2 and is Dependent on Interaction with miR-365.ADVANCED SCIENCE,5(7),9.
MLA	Gao, Ming,et al."LncRNA MT1DP Aggravates Cadmium-Induced Oxidative Stress by Repressing the Function of Nrf2 and is Dependent on Interaction with miR-365".ADVANCED SCIENCE 5.7(2018):9.